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• The Genomic Map of Polad in Open Access

  The main goal is to prepare and share WGS/WES of Polish population

  Study EGAS50000000113

• The Genomic Map of Polad in Open Access

  The main goal is to prepare and share WGS/WES of Polish population

  Study EGAS50000000112

• The Genomic Map of Polad in Open Access

  The main goal is to prepare and share WGS/WES of Polish population

  Study EGAS50000000111

• The Genomic Map of Polad in Open Access

  The main goal is to prepare and share WGS/WES of Polish population

  Study EGAS50000000110

• Whole_Genome_sequencing_of_rhabdomyosarcoma_tumour_tissue

  The aim of this study is to investigate the genomic landscape of human cancer.

  Study EGAS00001008277

• Crohn_s_Exome_Sequencing

  The aim is to find rare variants of intermediate penetrance in those at risk of Crohn's disease

  Study EGAS00001000385

• Orphan_Tumour_Study___RNAseq

  The aim of this study is to study the genomes of ultra rare childhood tumours

  Study EGAS00001002534

• Widespread hypertranscription in aggressive human cancers

  Cancers are often defined by the dysregulation of specific transcriptional programs; however, the importance of global transcriptional changes is less understood. Hypertranscription is the genome-wide increase in RNA output. Hypertranscription’s prevalence, underlying drivers and prognostic significance are undefined in primary human cancer. This is due in part to limitations of expression profiling methods, which assume equal RNA output between samples. Here, we developed a computational method to directly measure hypertranscription in 7,494 human tumors, spanning 31 cancer types. Hypertranscription is ubiquitous across cancer, especially in aggressive disease. It defines patient subgroups with worse survival, even within well-established subtypes. Our data suggest that loss of transcriptional suppression underpins the hypertranscriptional phenotype. Single-cell analysis reveals hypertranscriptional clones, which dominate transcript production regardless of their size. Finally, patients with hypertranscribed mutations have improved response to immune checkpoint therapy. Our results provide fundamental insights into gene dysregulation across human cancers and may prove useful in identifying patients that would benefit from novel therapies.

  Study EGAS00001006365

• DAC for achalasia risk consortium (arc)

  Dac EGAC00001000394

• DAC for aflatoxin project Qidong patient samples

  Dac EGAC00001000679

• DAC for the cfSort study (tissue deconvolution)

  Dac EGAC00001003222

• DAC for seminoma genomic data

  Dac EGAC00001000231

• DAC for study WES of pituitary tumors

  Dac EGAC00001000443

• Data Access Committee for Hui Lab

  Dac EGAC00001000454

• INRP - Italian Network for Research on Psychoses

  Dac EGAC00001000576

• DAC for MOMA, Short QT Exome data

  Dac EGAC00001000730

• DAC for Dissecting Tumor Microenvironment with Tumorgrafts

  Dac EGAC00001000809

• Data Access Committee for data from EGAS00001002840

  Dac EGAC00001000834

• DAC for human single nuclei RNAseq of Epilepsy

  Dac EGAC00001000860

• Data Access Committee for the CentralAfricanCMC_Pemberton dataset

  Dac EGAC00001000896

• Laboratory for Neurobiology (VIB-KU Leuven)

  Dac EGAC00001001282

• DAC for HSTCL study. National Cancer Centre Singapore.

  Dac EGAC00001001302

• DAC for MEITL study. National Cancer Centre Singapore.

  Dac EGAC00001001323

• DAC for Phylogenetic reconstruction of breast cancer

  Dac EGAC00001001572

• Center for Technology Licensing at Cornell University

  Dac EGAC00001001587